Sudden Cardiac Arrest

The causes differ markedly by age. In athletes under about 35, most arrests stem from inherited or congenital heart disease that predisposes to a sudden arrhythmia. Structural causes include hypertrophic cardiomyopathy (HCM) and arrhythmogenic cardiomyopathy (ACM); electrical causes include the inherited ion channelopathies such as long QT syndrome, Brugada syndrome and catecholaminergic polymorphic ventricular tachycardia; and congenital coronary artery anomalies and myocarditis account for further cases. In some young people the heart appears structurally normal even at post-mortem, a pattern termed sudden arrhythmic death syndrome. A distinct mechanical cause is commotio cordis, in which a blunt blow to the chest, for example from a cricket ball or a hockey ball, landing at a vulnerable point in the cardiac cycle triggers ventricular fibrillation in a structurally normal heart, a direct link between chest trauma in sport and cardiac arrest.

In older, masters athletes, the dominant cause shifts to coronary artery disease (CAD), where exertion precipitates ischaemia and a fatal arrhythmia. Across all ages the final common pathway is usually ventricular fibrillation or pulseless ventricular tachycardia, which is precisely why early defibrillation is so decisive.

An athlete in cardiac arrest collapses suddenly, is unresponsive and is not breathing normally. The single most important and most commonly missed point is that abnormal breathing is not the same as normal breathing. In the first minutes, slow, gasping or agonal breaths are frequent and are often misread as a sign of life, which delays CPR. Brief seizure-like jerking at the moment of collapse is also common and is regularly mistaken for a primary seizure, again delaying the correct response.

The working rule is simple and worth holding onto under pressure: if a collapsed athlete is unresponsive and not breathing normally, treat it as a cardiac arrest and act. Equally, an athlete who has an unexpected collapse but recovers quickly should still be removed from play, assessed promptly, and not allowed to continue that day.

Survival depends on a sequence often described as the chain of survival: early recognition and a call for help, early high-quality CPR, early defibrillation, and rapid handover to the ambulance service and hospital. The moment an arrest is recognised, call 999 on speakerphone, state clearly that this is a cardiac arrest, give the exact location, send someone for the nearest automated external defibrillator (AED), and send someone to meet and direct the ambulance.

Start chest compressions immediately in the centre of the chest. For an adult or larger adolescent, compress at about 100 to 120 per minute to a depth of 5 to 6 centimetres, allowing full recoil, and give 30 compressions to 2 rescue breaths if trained and able, otherwise continue compression-only CPR. For a younger child, use paediatric basic life support if trained: five initial rescue breaths, then 15 compressions to 2 breaths, with a compression depth of at least one third of the chest.

Keep CPR going while the AED pads are attached, and follow the device's spoken prompts. Pause only while it analyses the rhythm or delivers a shock, make sure nobody is touching the athlete at those moments, and restart compressions immediately afterwards. A paediatric AED setting can be used for small children if available, otherwise standard pads are used. Because the commonest rhythm is shockable, a defibrillator applied within the first few minutes is the single intervention most likely to save the athlete. In organised sport with a medical team, resuscitate where the athlete collapses unless the scene is unsafe, do not prioritise moving them over high-quality compressions and defibrillation, and where a shockable rhythm persists deliver repeated shocks on the field, commonly at least three, before transfer to an appropriate hospital.

Prevention works at two levels, and for most sports settings the first matters more than the second. The first is a venue genuinely prepared to respond: a written and rehearsed emergency action plan (EAP) that names who calls 999, who starts CPR and who fetches the defibrillator, with a signposted, accessible and maintained AED positioned so that the first shock, if indicated, can be delivered within about two minutes of collapse, and with staff trained in basic life support. This preparedness saves more lives than any test, because it shortens the time to CPR and defibrillation.

The second level is pre-participation cardiovascular screening. There is no universal NHS screening programme for all athletes in the UK; screening is used mainly in elite, academy, professional and charity-led settings, usually combining a personal and family history, a cardiovascular examination and a resting electrocardiogram (ECG) interpreted by clinicians experienced in athlete ECGs. It is not perfect, producing false positives and still missing some disease. For masters athletes, assessment should also address coronary risk factors and exertional symptoms, remembering that a normal resting ECG does not exclude coronary disease.

An athlete who survives an arrest needs urgent specialist cardiology assessment to establish the cause, because the underlying diagnosis drives everything that follows. Where the cause is unexplained or familial, this should involve a service with inherited cardiac conditions expertise. Investigation may include coronary assessment, cardiac magnetic resonance imaging, echocardiography, a 12-lead ECG, ambulatory rhythm monitoring, exercise testing, selected provocative testing, and genetic and family evaluation, so that first-degree relatives can be screened for the same condition.

Decisions about an implantable cardioverter defibrillator (ICD) and about whether and how to return to sport are specialist, individualised, and made with the athlete as a shared decision that weighs the diagnosis against the demands and risks of their sport. The role of the SEM clinician is to refer promptly, to support the athlete and family through a frightening time, and to reinforce that return to competition is a cardiology-led decision rather than something to be rushed.

• •Resuscitation Council UK guidance defines the chain of survival, basic life support and AED use that underpin the immediate response, including its best practice for resuscitation on the field of play.
• •European Society of Cardiology guidance on sports cardiology and pre-participation evaluation informs screening and return-to-sport decisions used in the UK.
• •National Institute for Health and Care Excellence (NICE) guidance on transient loss of consciousness supports red-flag assessment and urgent referral after exertional collapse.
• •Family and genetic evaluation after unexplained sudden cardiac arrest is guided through inherited cardiac conditions and NHS genomic medicine pathways, supported by charities such as Cardiac Risk in the Young (CRY).

• •Sudden cardiac arrest is the leading medical cause of sudden death in sport; survival falls with every minute before CPR and defibrillation.
• •Under about 35, inherited and congenital conditions dominate (hypertrophic and arrhythmogenic cardiomyopathy, ion channelopathies, coronary anomalies, myocarditis); in masters athletes, coronary artery disease.
• •Agonal or gasping breaths and brief seizure-like activity are easily mistaken for signs of life and delay CPR; treat unresponsive and not breathing normally as arrest.
• •The chain of survival is early recognition and a 999 call, early CPR, early defibrillation, and rapid handover.
• •Commotio cordis links a blunt chest blow to ventricular fibrillation in a structurally normal heart.
• •Exertional syncope, an abnormal electrocardiogram, and a family history of sudden death under 40 are red flags needing assessment before return.